Assessment of resting perfusion defect in patients with acute myocardial infarction: comparison of myocardial contrast echocardiography with contrast-enhanced magnetic resonance imaging

Abstract

Background: Contrast-enhanced magnetic resonance imaging (CE-MRI) can identify myocardial scarring following acute myocardial infarction (AMI).

Aim: To compare myocardial contrast echocardiography (MCE) and CE-MRI in detection of resting perfusion defect in patients with acute myocardial infarction.

Methods: Twenty four patients (21 men, 3 women, mean age 58.7 +/- 11.4 years) underwent primary percutaneous coronary angioplasty (PCI) for anterior AMI. All patients underwent MCE: segmental perfusion was estimated in real time before and immediately after PCI and on third day after PCI, using low mechanical index (0.3) after 0.3-0.5 ml bolus injections of intravenous OptisonTM. The MCE was scored semiquantitatively as: 1--homogenous contrast enhancement, 2--patchy contrast enhancement, 3--no contrast (non-viable myocardium). All patients underwent CE-MRI on a 1.5 T scanner (SONATA, Siemens) on the third day after PCI. Acquisition of short axis slices was performed before and 20 min after injection of Gd-DPTA (0.15 mmol/kg) with an inversion recovery TurboFLASH sequence (TE 1.1 ms, TR 700 ms, flip angle 300) in multiple breath-holds. The pattern of hyperenhancement representing MI (which intensity was more than 150% intensity of myocardium) was quantified by planimetry. The CE-MRI was scored according to the severity of myocardial scar as: 1--without scar, 2-- <50% of myocardial thickness, 3 - > 50% of myocardial thickness.

Results: Myocardial perfusion was analysed using MCE and contrast-enhanced MRI in 362 segments. Agreement between MCE and CE-MRI for identification of viable versus necrotic myocardium on third day after PCI was 86% (kappa = 0.73). Thirteen (54%) patients showed transmural necrosis at CE-MRI while 11 (46%) showed non-transmural necrosis. Patients from the transmural necrosis group showed a higher creatine kinase peak (p = 0.0001), higher CK-MB (p = 0.00002) and higher troponine level (p = 0.008), and more impaired baseline regional contractile function (p = 0.045). All angiographic parameters were less favourable in this group before as well as after PCI than in patients with non-transmural necrosis.

Conclusions: Myocardial contrast echocardiography correlates very well with CE-MRI in the assessment of myocardial perfusion after PCI in AMI. Contrast-enhanced MRI is accurate technique for assessing the infarct zone. Identification by CE-MRI of transmural necrosis was associated with more impaired left ventricular function, non-reperfused MI, and presence of Q waves in ECG.